Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons.
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Association between tetrodotoxin resistant channels and lipid rafts regulates sensory neuron excitabilityTemperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7A single sodium channel mutation produces hyper- or hypoexcitability in different types of neuronsSynthetic ciguatoxins selectively activate Nav1.8-derived chimeric sodium channels expressed in HEK293 cellsThe Brugada Syndrome: A Rare Arrhythmia Disorder with Complex InheritancePrimary erythromelalgia: a reviewThe perception and endogenous modulation of painRoles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic NeuropathyTMEM16C facilitates Na(+)-activated K+ currents in rat sensory neurons and regulates pain processingRelationship of axonal voltage-gated sodium channel 1.8 (NaV1.8) mRNA accumulation to sciatic nerve injury-induced painful neuropathy in ratsVoltage-gated sodium channel in grasshopper mice defends against bark scorpion toxinNovel loci associated with PR interval in a genome-wide association study of 10 African American cohortsA gain-of-function voltage-gated sodium channel 1.8 mutation drives intense hyperexcitability of A- and C-fiber neurons.Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a.Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.Adrenergic stimulation mediates visceral hypersensitivity to colorectal distension following heterotypic chronic stress.Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators.Aquaporin-1 tunes pain perception by interaction with Na(v)1.8 Na+ channels in dorsal root ganglion neurons.Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice.Phenotyping sensory nerve endings in vitro in the mouse.Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disordersContribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.Antisense-mediated knockdown of Na(V)1.8, but not Na(V)1.9, generates inhibitory effects on complete Freund's adjuvant-induced inflammatory pain in rat.Transmembrane segments prevent surface expression of sodium channel Nav1.8 and promote calnexin-dependent channel degradationA nonsense mutation in the SCN9A gene in congenital insensitivity to painExpression of 5-HT3 receptors and TTX resistant sodium channels (Na(V)1.8) on muscle nerve fibers in pain-free humans and patients with chronic myofascial temporomandibular disorders.Gain-of-function Nav1.8 mutations in painful neuropathy.Combined small-molecule inhibition accelerates developmental timing and converts human pluripotent stem cells into nociceptors.Exon 11 skipping of SCN10A coding for voltage-gated sodium channels in dorsal root gangliaInhibition of tetrodotoxin-resistant sodium current in dorsal root ganglia neurons mediated by D1/D5 dopamine receptorsCalmodulin regulates current density and frequency-dependent inhibition of sodium channel Nav1.8 in DRG neurons.Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders.A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.The roles of sodium channels in nociception: Implications for mechanisms of painFunctional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone painSCN10A/Nav1.8 modulation of peak and late sodium currents in patients with early onset atrial fibrillationAlterations of action potentials and the localization of Nav1.6 sodium channels in spared axons after hemisection injury of the spinal cord in adult rats.A sensory subpopulation depends on vesicular glutamate transporter 2 for mechanical pain, and together with substance P, inflammatory pain
P2860
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P2860
Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons.
description
2001 nî lūn-bûn
@nan
2001 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Contribution of Na
@nl
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@ast
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@en
type
label
Contribution of Na
@nl
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@ast
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@en
prefLabel
Contribution of Na
@nl
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@ast
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@en
P2093
P356
P1476
Contribution of Na(v)1.8 sodiu ...... electrogenesis in DRG neurons.
@en
P2093
Cummins TR
Renganathan M
P304
P356
10.1152/JN.2001.86.2.629
P407
P577
2001-08-01T00:00:00Z